Fusarium head blight resistance in European winter wheat: insights from genome-wide transcriptome analysis.

BACKGROUND: Fusarium head blight (FHB) is a devastating disease of wheat worldwide. Resistance to FHB is quantitatively controlled by the combined effects of many small to medium effect QTL. Flowering traits, especially the extent of extruded anthers, are strongly associated with FHB resistance. RESULTS: To characterize the genetic basis of FHB resistance, we generated and analyzed phenotypic and gene expression data on the response to Fusarium graminearum (Fg) infection in 96 European winter wheat genotypes, including several lines containing introgressions from the highly resistant Asian cultivar Sumai3. The 96 lines represented a broad range in FHB resistance and were assigned to sub-groups based on their phenotypic FHB severity score. Comparative analyses were conducted to connect sub-group-specific expression profiles in response to Fg infection with FHB resistance level. Collectively, over 12,300 wheat genes were Fusarium responsive. The core set of genes induced in response to Fg was common across different resistance groups, indicating that the activation of basal defense response mechanisms was largely independent of the resistance level of the wheat line. Fg-induced genes tended to have higher expression levels in more susceptible genotypes. Compared to the more susceptible non-Sumai3 lines, the Sumai3-derivatives demonstrated higher constitutive expression of genes associated with cell wall and plant-type secondary cell wall biogenesis and higher constitutive and Fg-induced expression of genes involved in terpene metabolism. Gene expression analysis of the FHB QTL Qfhs.ifa-5A identified a constitutively expressed gene encoding a stress response NST1-like protein (TraesCS5A01G211300LC) as a candidate gene for FHB resistance. NST1 genes are key regulators of secondary cell wall biosynthesis in anther endothecium cells. Whether the stress response NST1-like gene affects anther extrusion, thereby affecting FHB resistance, needs further investigation. CONCLUSION: Induced and preexisting cell wall components and terpene metabolites contribute to resistance and limit fungal colonization early on. In contrast, excessive gene expression directs plant defense response towards programmed cell death which favors necrotrophic growth of the Fg pathogen and could thus lead to increased fungal colonization.

Genetic factors affecting Fusarium head blight resistance improvement from introgression of exotic Sumai 3 alleles (including Fhb1, Fhb2, and Fhb5) in hard red spring wheat.

BACKGROUND: Fusarium head blight resistance genes, Fhb1 (for Type-II resistance), Fhb2 (Type-II), and Fhb5 (Type-I plus some Type-II), which originate from Sumai 3, are among the most important that confer resistance in hexaploid wheat. Near-isogenic lines (NILs), in the CDC Alsask (susceptible; n = 32) and CDC Go (moderately susceptible; n = 38) backgrounds, carrying these genes in all possible combinations were developed using flanking microsatellite markers and evaluated for their response to FHB and deoxynivalenol (DON) accumulation in eight environments. NILs were haplotyped with wheat 90 K iSelect assay to elucidate the genomic composition and confirm alleles' presence. Other than evaluating the effects of three major genes in common genetic background, the study elucidated the epistatic gene interactions as they influence FHB measurements; identified loci other than Fhb1, Fhb2, and Fhb5, in both recurrent and donor parents and examined annotated proteins in gene intervals. RESULTS: Genotyping using 81,857 single nucleotide polymorphism (SNP) markers revealed polymorphism on all chromosomes and that the NILs carried < 3% of alleles from the resistant donor. Significant improvement in field resistance (Type-I + Type-II) resulted only among the CDC Alsask NILs, not the CDC Go NILs. The phenotypic response of NILs carrying combinations of Sumai 3 derived genes suggested non-additive responses and Fhb5 was as good as Fhb1 in conferring field resistance in both populations. In addition to Fhb1, Fhb2, and Fhb5, four to five resistance improving alleles in both populations were identified and three of five in CDC Go were contributed by the susceptible parent. The introgressed chromosome regions carried genes encoding disease resistance proteins, protein kinases, nucleotide-binding and leucine rich repeats' domains. Complex epistatic gene-gene interactions among marker loci (including Fhb1, Fhb2, Fhb5) explained > 20% of the phenotypic variation in FHB measurements. CONCLUSIONS: Immediate Sumai 3 derivatives carry a number of resistance improving minor effect alleles, other than Fhb1, Fhb2, Fhb5. Results verified that marker-assisted selection is possible for the introgression of exotic FHB resistance genes, however, the genetic background of the recipient line and epistatic interactions can have a strong influence on expression and penetrance of any given gene.

Metabolomics deciphers the host resistance mechanisms in wheat cultivar Sumai-3, against trichothecene producing and non-producing isolates of Fusarium graminearum.

Fusarium head blight (FHB) of wheat, caused by Fusarium graminearum, reduces grain yield and contaminates grains with trichothecene mycotoxins. Host resistance to FHB is quantitatively inherited and more than 100 QTLs have been mapped, but the host resistance mechanisms are poorly understood. Non-targeted metabolic profiling was applied to elucidate the host resistance mechanisms to FHB spread through rachis of wheat cultivar Sumai-3 against both trichothecene producing and non-producing isolates of Fusarium graminearum. The accumulation of deoxynivalenol (DON) in Sumai-3 was low, however the resistance to spread was not due to its detoxification into DON-3-O-glucoside (D3G), as the proportion of total DON converted to D3G in the resistant was not significantly different from that in the susceptible cultivar Roblin. Instead, the resistance was considered to be due to the accumulation of resistance related (RR) metabolites belonging to the phenylpropanoid pathway that reduced pathogen advancement through increased host cell wall thickening and also reduced pathogen growth due to antifungal and/or antioxidant properties which, in turn, reduced subsequent trichothecene biosynthesis. The RR phenylpropanoids accumulated in Sumai-3 were mainly the preformed syringyl rich monolignols and their glucosides, which are precursors of lignin biosynthesis, as well as antimicrobial flavonoids. The resistant cultivar Sumai-3 inoculated with trichothecene producing F. graminearum not only accumulated less RR metabolites but also the abundance of many RR metabolites was lesser than in the trichothecene non-producing F. graminearum. This implies repression of host resistance mechanisms by trichothecenes/DON, which is a protein biosynthesis inhibitor. Enhancement of resistance in wheat against FHB can be exploited through stacking of candidate phenylpropanoid pathway genes.